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Aging of living organisms is governed by intrinsic developmental programs, of which progression is often under the regulation of their cellular energy status. For example, calorie restriction is known to slow down aging of heterotrophic organisms from yeasts to mammals. In autotrophic plants cellular energy deprivation by perturbation of photosynthesis or sugar metabolism is also shown to induce senescence delay. However, the underlying molecular and biochemical mechanisms remain elusive. Our plant cell-based functional and biochemical assays have demonstrated that SNF1-RELATED KINASE1 (SnRK1) directly interacts, phosphorylates, and destabilizes the key transcription factor ETHYLENE INSENSITIVE3 (EIN3) in senescence-promoting hormone ethylene signaling. Combining chemical manipulation and genetic validation using extended loss-of-function mutants and gain-of-function transgenic lines, we further revealed that a SnRK1 elicitor, 3-(3,4-dichlorophenyl)-1,1-dimethylurea enables to slow down senescence-associated leaf degreening through the regulation of EIN3 in  Arabidopsis . Our findings enlighten that an evolutionary conserved cellular energy sensor SnRK1 plays a role in fine-tuning of organ senescence progression to avoid sudden death during the last step of leaf growth and development.

Regulatory Functions of Cellular Energy Sensor SNF1-Related Kinase1 for Leaf Senescence Delay through ETHYLENE- INSENSITIVE3 Repression